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学科主题临床医学
CSTP1, a Novel Protein Phosphatase, Blocks Cell Cycle, Promotes Cell Apoptosis, and Suppresses Tumor Growth of Bladder Cancer by Directly Dephosphorylating Akt at Ser473 Site
Zhuo, De-Xiang1,4; Zhang, Xiao-Wei1; Jin, Bo1; Zhang, Zheng2,3; Xie, Bu-Shan1; Wu, Cheng-Lin1; Gong, Kan2,3; Mao, Ze-Bin1
刊名PLOS ONE
2013-06-17
DOI10.1371/journal.pone.0065679
8期:6
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Multidisciplinary Sciences
研究领域[WOS]Science & Technology - Other Topics
关键词[WOS]KINASE-B ; 3-KINASE PATHWAY ; FGFR3 MUTATIONS ; GENE-MUTATIONS ; ACTIVATION ; CARCINOMA ; PHOSPHORYLATION ; IDENTIFICATION ; PTEN/MMAC1 ; PHLPP
英文摘要

Akt/protein kinase B is a pivotal component downstream of phosphatidylinositol 3-kinase (PI3K) pathway, whose activity regulates the balance between cell survival and apoptosis. Phosphorylation of Akt occurs at two key sites either at Thr308 site in the activation loop or at Ser473 site in the hydrophobic motif. The phosphorylated form of Akt (pAkt) is activated to promote cell survival. The mechanisms of pAkt dephosphorylation and how the signal transduction of Akt pathway is terminated are still largely unknown. In this study, we identified a novel protein phosphatase CSTP1(complete s transactivated protein 1), which interacts and dephosphorylates Akt specifically at Ser473 site in vivo and in vitro, blocks cell cycle progression and promotes cell apoptosis. The effects of CSTP1 on cell survival and cell cycle were abrogated by depletion of phosphatase domain of CSTP1 or by expression of a constitutively active form of Akt (S473D), suggesting Ser473 site of Akt as a primary cellular target of CSTP1. Expression profile analysis showed that CSTP1 expression is selectively down-regulated in non-invasive bladder cancer tissues and over-expression of CSTP1 suppressed the size of tumors in nude mice. Kaplan-Meier curves revealed that decreased expression of CSTP1 implicated significantly reduced recurrence-free survival in patients suffered from non-invasive bladder cancers.

语种英语
WOS记录号WOS:000321397800014
项目编号81272827 ; 30971627
资助机构National Science Foundation of China
引用统计
被引频次:5[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/56435
专题北京大学第一临床医学院_泌尿外科
北京大学基础医学院
作者单位1.Peking Univ, Hosp 1, Dept Urol, Beijing 100871, Peoples R China
2.Peking Univ, Inst Urol, Beijing 100871, Peoples R China
3.Peking Univ, Hlth Sci Ctr, Dept Biochem & Mol Biol, Beijing 100871, Peoples R China
4.Fujian Med Univ, Hosp Sanming 1, Dept Lab Med, Sanming, Fujian, Peoples R China
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Zhuo, De-Xiang,Zhang, Xiao-Wei,Jin, Bo,et al. CSTP1, a Novel Protein Phosphatase, Blocks Cell Cycle, Promotes Cell Apoptosis, and Suppresses Tumor Growth of Bladder Cancer by Directly Dephosphorylating Akt at Ser473 Site[J]. PLOS ONE,2013,8(6).
APA Zhuo, De-Xiang.,Zhang, Xiao-Wei.,Jin, Bo.,Zhang, Zheng.,Xie, Bu-Shan.,...&Mao, Ze-Bin.(2013).CSTP1, a Novel Protein Phosphatase, Blocks Cell Cycle, Promotes Cell Apoptosis, and Suppresses Tumor Growth of Bladder Cancer by Directly Dephosphorylating Akt at Ser473 Site.PLOS ONE,8(6).
MLA Zhuo, De-Xiang,et al."CSTP1, a Novel Protein Phosphatase, Blocks Cell Cycle, Promotes Cell Apoptosis, and Suppresses Tumor Growth of Bladder Cancer by Directly Dephosphorylating Akt at Ser473 Site".PLOS ONE 8.6(2013).
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